Role of Tumor Necrosis Factor-α, Interleukin-8, and Dexamethasone in the Focal Adhesion Kinase Expression by Human Nucleus Pulposus Cells

In Brief Study Design. Human nucleus pulposus cells from intervertebral disc specimens were cultured to study the effects of tumor necrosis factor (TNF)-α and interleukin (IL)-8 on the focal adhesion kinase (FAK) expression by these cells. The effect of co-stimulation with dexamethasone on the FAK expression by nucleus pulposus cells was also studied. Objectives. To evaluate the possible role of activated FAK expressed by the human nucleus pulposus cells and its correlation with inflammatory cytokines (TNF-α, IL-8) and dexamethasone. Summary of Background Data. There have been no reported studies showing the correlation between the activated FAK expression by human nucleus pulposus cells with inflammatory cytokines and dexamethasone. Methods. The FAK expression in cultured human nucleus pulposus cells was studied, and Western blot and immunofluorescence analysis were performed to assess its relation to TNF-α, IL-8, and dexamethasone. Results. Treatments of TNF-α and IL-8 up-regulated the activated FAK expression. Dexamethasone attenuated the cytokine-induced FAK expression. The effects of inflammatory cytokines on the FAK expression were found to be concentration dependent, with greater correlation shown by IL-8 than TNF-α. Conclusion. TNF-α and IL-8 stimulation up-regulated the FAK expression of human nucleus pulposus cells, and the coadministration of dexamethasone attenuated it. Human nucleus pulposus cells were studied for the effects of tumor necrosis factor (TNF)-α, interleukin (IL)-8, and dexamethasone on the focal adhesion kinase (FAK) expression. TNF-α and IL-8 up-regulated the FAK expression, whereas dexamethasone attenuated the FAK expression when it was given with TNF-α and IL-8. Activated FAK might play a role in events leading to disc degeneration.